The primary objective of this investigation is to identify a neurophysiologic correlate for subjective tinnitus, a clinical phenomenon most often produced by cochlear injury or disruption of the cochlear nerve. Development of such a correlate is based upon the hypothesis that tinnitus represents spontaneous neuronal activity along the central auditory pathway and that such aberrant activity arises in response to cochlear injury but independently of acoustic stimulation. Such a correlate can be developed through the quantitative identification of spontaneous neuronal activity within the central auditory pathway, using 14C 2-deoxyglucose in functional mapping of the brain. If a tinnitus correlate is verified in this way, acoustic, pharmacologic, and electrophysiologic methods of modifying it may have important therapeutic implications. It is hoped that data obtained in response to auditory de-afferentation may provide clues etiologically significant to an otologic symptom for which there is yet no clear understanding and therefore no effective therapy.